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Both, the presence of infections as well as the impact of shear stress and oxygen toxicity, independently increase lung elastase and protease activity in the developing lung, due to the accentuated release from cellular and matrix sources.
To meet the therapeutic goal of focal adenosine augmentation, genetic disruption of the adenosine metabolizing enzyme, adenosine kinase (ADK) in rodent cells was used as a molecular strategy to induce adenosine release from cellular brain implants, which demonstrated antiepileptic and neuroprotective properties.
To meet the therapeutic goal of focal adenosine augmentation, genetic disruption of the adenosine metabolizing enzyme adenosine kinase (ADK) in rodent and human cells was used as a molecular strategy to induce adenosine release from cellular brain implants, which demonstrated antiepileptic and neuroprotective properties.
Hence, characterizations of ischemia as somehow transforming water from gel-like to free or causing water release from cellular proteins seem unsound.
On the other hand, the low correlation may indicate a selective penetration of the enzymes as a result of their degranulation and release from cellular lysosomes.
The leukotriene pathway including the enzyme responsible for arachidonic acid release from cellular phospholipids, cPLA2α, is a major contributor to asthmatic responses and an attractive target in asthma therapies.
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Besides arachidonic acid released from cellular membranes for eicosanoid synthesis, several if not all sPLA2s have recently been implicated in hydrolysis of phospholipids in lipoprotein particles.
Based on the facts that FAs sequester proteins involved in SG nucleation and RNAs released from cellular translational machinery, one would expect them to interfere with SG formation under stress.
With this process, enzymes were used for cell disruption and for catalyzing product release from internal cellular compartments.
Extracellular release from hemoproteins, cellular uptake, and intracellular metabolism determine the cumulative exposure of cells and tissues to heme.
n-3 PUFA may also regulate other complex metabolic processes, including β-oxidation, lipid release from glycerophospholipids, cellular signaling of membrane bound proteins, eicosanoid synthesis, and direct activation of nuclear receptors and gene transcription, all of which may influence the development and progression of prostate cancer.
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